- Dec 2021
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When describing her husband, Anna thinks, “He’s not a man, not a human being, he’s a puppet. Nobody else knows it, but I do...He’s not a man, he’s an administrative machine” (360). In the process of trying to justify her crime, Anna dehumanizes her husband, making him into a mere puppet that can be hurt without fear. For if her crime only affects one without a heart, can it be considered a crime at all? The student that Raskolnikov overhears uses a similar logical technique when he says, “And what does the life of this stupid, consumptive, and wicked old crone mean in the general balance? No more than the life of a louse, a cockroach, and not even that much, because the old crone is harmful”
Both Anna and Raskolnikov justify their crimes by making the person they are transgressing against seem to be not human at all. Of course, crimes can only be committed on humans.
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- Oct 2021
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Nutrition educators can also use an indirect route to address environmental determinants. The indirect route involves unconscious and conscious processes (Kremers et al. 2006). Unconscious processes operate through an automatic or “mindless” route in which the behaviors are automatically elicited by the environment through established environment-behavior links. For nutrition education, a behavioral economics approach has much to offer for taking advantage of unconscious processes.
This is based off the idea that where foods are placed in venues as well as how they look has a large determination on if people will buy them or not.
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Although food neophobia, or fear of new foods, is mini-mal in infants, it increases through early childhood so that 2- to 5-year-olds, like other young omnivores, demonstrate neophobia (Birch 1999; Dovey et al. 2008). This would have adaptive value because infants are fed by adults, whereas toddlers are beginning to explore their world and have not learned yet what is safe to eat and what is not. However, neophobia can be reduced by repeated opportunities to sample new foods
Infants are fine with new foods where as toddlers start to develop Neophobia because they are starting to explore the environment away from the parents.
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The school food environment can have a largeimpact on children’s and adolescents’ dietaryintake because up to two meals and snacksare eaten at school every day (91). Food atschool is typically available through federallyreimbursed school meals and “competitivefoods,” so called because they compete withthe school meals program. Competitive foodsare all foods and beverages sold outside of thefederal meal programs and include vendingmachines, a la carte offerings in the cafete-ria, snack bars, school stores, and fundraisers
In order to fight obesity, the competitive foods that are offered at school should be fruits and vegetables rather than soda and chips.
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Telomeres with long lengths are considered protective against chronic diseases and earlier death, whereas short lengths increase risk. Antioxidants can help combat cell stress and preserve telomere length, such as by eating foods that contain antioxidants nutrients like fruits, vegetables, nuts, and whole grains. These foods are found in healthy eating patterns like the Mediterranean diet. [12] This was demonstrated in a large cohort of 4676 healthy middle-aged women from the Nurses’ Health Study where participants who more closely followed the Mediterranean diet were found to have longer telomere length.
The Mediterranean diet might help aid in longer age by making decreasing the rate at which Telomers shorten from cell growth and division.
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The Mediterranean diet is a primarily plant-based eating plan that includes daily intake of whole grains, olive oil, fruits, vegetables, beans and other legumes, nuts, herbs, and spices. Other foods like animal proteins are eaten in smaller quantities, with the preferred animal protein being fish and seafood.
Although the pyramid shape suggests the proportion of foods to eat (e.g., eat more fruits and vegetables and less dairy foods), it does not specify portion sizes or specific amounts. It is up to the individual to decide exactly how much food to eat at each meal, as this will vary by physical activity and body size.
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. If this continues for 3-4 days and stored glucose is fully depleted, blood levels of a hormone called insulin decrease, and the body begins to use fat as its primary fuel. The liver produces ketone bodies from fat, which can be used in the absence of glucose.
If the body continues to pull stored glucose during fasting or when very little carbohydrates are eaten, this is what happens.
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Wisdom et al. (2010) took a different approach to measuringthe impact of calorie information on fast food orders; they con-ducted a randomized field experiment in which customers enteringa fast food sandwich restaurant were offered a free meal (consist-ing of a sandwich, side dish, and drink) in exchange for completinga survey. Subjects (N = 638) chose their free meal from a menu, arandom subset of which contained calorie information. Regressionestimates indicate that the provision of calorie information on themenu altered meal choice such that calories ordered fell by 60.7.Calories from the sandwich did not change – the reduction was dueto changes in the side dish and drink.
The results of this study suggest that people may be inelastic to calorie information when ordering the primary food item at a store. Sandwiches at Starbucks for instance. They will, however, take the calorie information into account when ordering side items. The problem with the study was that they didn't look into how many calories were actually consumed from what the people ordered.
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olicies that induce the food industry to redesign foods maybe more effective than policies that rely entirely on inducing response by consumers. Policies thatcombine the push of market incentives with the pull of public education and childhood obesityprevention policies may be best of all, but for now, this is little more than conjecture.
Policies that might be helpful to fight obesity
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Income is another determinant of choices regarding food and physical activity. Economictheory predicts an inverted U-shaped relationship between income and body weight (Lakdawalla& Philipson 2009, Philipson & Posner 2003). The very poor are hungry and undernourished, andas their incomes increase, individuals increase their consumption of food, thus increasing theirbody weight. Beyond a certain threshold, however, increases in body weight begin to lower utility,and individuals try to increase their food expenditure and food consumption without gainingbody weight. Consistent with this theory, obesity prevalence falls with income and educationin developed countries and rises with income in developing nations (McLaren 2007, Sobal &Stunkard 1989).
High income in developing nations actually positively correlates with obesity where as high income in developed nations negatively correlates with obesity.
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An increase in a woman’s hours employed in market work could increase her body weight andthat of her family in two ways.
One way is she has less time to prepare home cooked meals which will be replaced by unhealthy processed food. Second she has less time to supervise the child which means children will be more likely to engage in unhealthy behaviors like eating unhealthy foods, watching television, and sleeping less.
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- Sep 2021
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In studies conducted in the United States, African Americans exhibited a higher prevalence of extreme obesity than other ethnicities22. Asian populations have lower BMI values than white individuals, but they have been shown to be prone to visceral fat deposition, making Asian populations more susceptible to develop-ing type 2 diabetes mellitus at lower BMI levels than white individuals
African Americans exhibit the highest levels of obesity in the United States where as Asian populations exhibit the lowest level of obesity.
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Undoubtedly, more attention and financial support should be paid to the prevention of obesity19. At the popu-lation level, public policies and economical strategies are needed to improve food and physical environments, the food system and the health system to curb the global obesity epidemic.
Some things being done to help prevent obesity are the raising of taxes on sugary drinks, a changing of television hours to promote sleep and physical activity, and motivational interviewing techniques.
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Use of bariatric surgery (also known as metabolic sur-gery) has become rapidly adopted as a treatment option for severe obesity, and this has increased with the advent of lower-risk laparoscopic procedures
The surgery makes patients less hungry by placing a band around the entrance to the stomach. This leads to less calories being eaten in a day.
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A large-scale study revealed that the absolute value of visceral fat area correlated with obesity-associated cardiovascular risks, but cardiovascular risks did not increase with the increase of subcutaneous fat223. Accordingly, adipose tissues in subcutaneous fat obesity might function normally with the expected release of anti-inflammatory adipokines, whereas adipose tissues in visceral fat obesity release an increased amount of pro-inflammatory adipokines and suppress the secretion of anti-inflammatory adipocytokines, thereby creating low-grade inflammation, which contributes to systemic metabolic and cardiovascular impairment that is associated with obesity-related disorders
Visceral fat is so much worse than subcutaneous fat because visceral fat adipose tissue releases Pro-Inflammatory adipokines while suppressing Anti-inflammatory adipokines.
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An increase in intraabdominal pressure purportedly accounts for the elevated risks of gastroesopha-geal ref lux disease, Barrett’s esophagus, and esophageal adenocarcinoma among persons who are overweight or obese.
The pressure on the gut brought about by obesity can bring many problems like GERD.
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Excess adiposity also imposes a mechanical load on joints, making obesity a risk factor for the development of osteoarthritis.2
Obesity can also lead to osteoarthritis by adding load on the joints
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Obesity is often accompanied by an in-crease in pharyngeal soft tissues, which can block airways during sleep and lead to obstruc-tive sleep apnea.
Obesity can lead to sleep apnea by blocking pharyngeal soft tissue airways.
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Adipose tissue surrounds the kidney, and the blood-pressure increase with renal compression may contribute to the hyper-tension frequently observed in patients who are obese.
Visceral tissue around the kidneys can lead to increased renal compression and in effect hypertension.
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Not all people exposed to prevailing urban and rural environments become obese, which suggests the existence of underlying genetic mechanisms operating at the individual level. Although estimates vary, twin, family, and adoption studies show that the rate of heritability of BMI is high, ranging from 40 to 70%.1
Obesity is a highly genetic disease.
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Almost all human data on the homeostatic and hedonic system arederived from cross-sectional studies, which do not support conclusionson causality. It is still debated whether the described changes in obesityare theresultof (long-term) obesity orpredisposeto a positive energybalance and weight gain.
More longitudinal or cross-sequential studies will need to be done before causality can be made in lots of obesity related correlations.
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Gut microbiota, often referred to as a separate metabolic organ[212], facilitate the digestion of dietary components, including thosecomponents that the innate digestive system cannot process. Gut mi-crobiota thereby increase the efficiency of energy harvest from ingestednutrients [213], and it has been hypothesized that gut microbiotacontribute to weight gain through this mechanism
Increased nutrient absorption from the gut microbiome can actually be bad in our society by allowing us to extract more calories from the same foods. This can lead to weight gain.
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Leptin is predominantly secreted by white adipose tissue. Circulat-ing levels correlate with fat mass and represent a hormonal signal ofbody energy stores [162–165]. In individuals with more body fat,serum, plasma and cerebrospinalfluid leptin levels are elevated [165].Leptin binds to its receptors, primarily relaying information on energystatus [165–168], but also on acute energy availability [169–171]. Inthe hypothalamus, leptin mediates most of its actions
Leptin increases in excretion in individuals with more body fat.
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The two major systems that control food intake are often referredto as the homeostatic and hedonic pathways [102]. The homeostaticpathway stimulates eating behavior when energy stores are low. Thehypothalamus and brainstem have been identified as its centers.Here, central and peripheral signals, including circulating concentra-tions of nutrients, gastrointestinal hormones, insulin, leptin, andvagal afferents, are integrated to mediate feelings of hunger vs satietyand adjust food intake. The hedonic, or reward-based, pathway addsanother layer of control and may override the homeostatic system[102].By mediating the rewarding and motivational aspects of food intake,the hedonic system can support energy homeostasis during periodsof relative energy deficiency, but also increase the intake of highlypalatable food during periods of relative energy sufficiency
The hedonic system was meant to help when we were still hunter gatherers and might need the food stores for later. In our mostly abundant food environment, however, it actually causes overconsumption problems.
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Both the homeostatic and hedonic regulatory systems receive inputfrom multiple signals that convey information on energy intake, currentenergy status, and long-term energy stores. These signals close theenergy expenditure-intake feedback loop and are therefore essentialfor the maintenance of energy balance. Obesity is associated withseveral changes in nutritional feedback
Obese people might have a skewed feedback between the homeostatic and hedonic pathways.
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Insulin-sensitive individuals have a more pronounced ther-mic effect of food, whereas the most insulin-resistant individuals havenegligible effects
People with high insulin resistance might be more prone to obesity as they burn less calories through the thermic effect of food.
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AEE can be categorized into exercise activity thermogenesis (EAT)and non-exercise activity thermogenesis (NEAT) [2]. Generally, the con-tribution of EAT to total daily EE is negligible [32], and NEAT is predom-inant [8]. NEAT comprises EE during all physical activities other thansport-like exercises, such as occupational EE and leisure-time physicalactivity [32]. It varies widely across and within individuals on a dailybasis and can differ up to 2000 kcal/day betweentwo individuals of sim-ilar size [32]. The variability in NEAT is in part genetically determined[33].
NEAT is actually a much larger part of our physical activity calorie expenditure than normal exercise.
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Overweight and obesity are characterized by excess amounts ofbody fat. They are usually defined as body mass index (BMI)≥25and≥30 kg/m2, respectively, although BMI does not differentiatebetween lean and fat mass and provides no information on body fatdistribution.
BMI, while easy to calculate, seems to be a poor indication of health risk because it doesn't distinguish between fat and muscle and doesn't take into account fat distribution.
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The prevalence of obesity was lower among non-Hispanic Asian adults (12.7%) compared with all other race and Hispanic-origin groups.
Non-Hispanic Asians have a much lower rate of obesity which could be because of their culture.
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